Cobalamin (Vitamin B-12) deficiency can be readily induced in fruit bats (Rousettus aegypticus) which are deprived of a dietary source of the vitamin in captivity. They develop an illness which resembles some of the complications of human pernicious anemia. This is characterized by neuropathy but not by hematologic complications. The specificity and suitability of this potential animal model for studying human cobalamin deficiency will be further investigated. Critical nutritional studies are being extended in order to confirm that cobalamin can prevent, arrest and reverse the neurological changes. Morphologic and biochemical studies will be carried out on cobalamin-deficient and cobalamin-replete bats. Evidence for demyelination will be sought by ultrastructural analytical methods. The integrity of cobalamin-dependent enzyme reactions will be measured in nervous and other tissues during induction of cobalamin deficiency. Attempts will be made to hasten or aggravate the onset and manifestations of cobalamin deficiency by various meams including the use of cobalamin analogs. Some bats will be treated with nitrous oxide, a putative cobalamin antagonist, and the effects of this treatment will be compared with the pure nutritional model. This project seeks to elucidate the metabolic role of cobalamin in nervous and other tissues and its interaction with other nutrients, notably folate.